Oxford neuroscience was splashed across the media this week with new research suggesting that atypical brain activity, caused by a high-risk Alzheimer’s disease gene, can be spotted as early as age twenty.

The study was performed in collaboration with Imperial College London and is published in Proceedings of the National Academy of Science. It shows a significant correlation between having the high-risk mutation of the gene in question, ApoE4, and a raised level of activity in the hippocampus, the part of the brain involved in memory formation. The researchers suggest that over-activity may simply wear that part of the brain out, leading to damage, and memory problems, in later life.

Alzheimer’s disease is a headline-grabber, and BBC News, The Telegraph and The Daily Mail (to name but a few) reported the findings accordingly. They detailed how this work could bring us close to a simple method of identifying those at increased risk of dementia early enough to offer prophylactic treatment.

However, these media reports are misleading. Firstly, the most important link that would allow the conclusions above to be drawn has not been demonstrated at all: we do not know whether this increased hippocampal activity is in fact linked to the actual development of Alzheimer’s disease or not.

MRI brain scan

Of course, it would take an investigation spanning half a century to show whether these mutation-carrying participants with increased brain activity at age 20-30 are more likely to develop dementia at age 70-80. But without evidence of this sort, it is entirely premature to suggest that this increased activity could be a helpful diagnostic tool.

And similarly, without this evidence, it is also premature for both the researchers and the media reports to say that over-activity in the hippocampus could be “effectively wearing it out”.

Secondly, even if it were to be shown that this higher activity is indeed linked to the future development of dementia, the diagnostic brain-scanning of all 20-30 year-olds with the rogue gene (around 25% of them) would be anything but the “simple test” that some of the articles would have you believe. These functional magnetic resonance imaging (fMRI) scans take about an hour to do and are very expensive: around £1500 a pop, plus the million quid you need to buy the scanner in the first place. Furthermore, these scans would have to exclude many potential participants, such as women who are pregnant, or could be pregnant, and anyone with metal inside their body, from a pacemaker to a surgical staple.

Lastly, even if this were a practical method of screening, an the ethical queston is raised by distinguishing, at an early age, those who are more likely to go on to develop Alzheimer’s disease. Fair enough, people found to be at risk could be offered early treatment and lifestyle advice. Unfortunately, there is currently no successful “early” or preventative treatment available, and neither do we know which lifestyle factors contribute to increased risk of Alzheimer’s disease, beyond the usual “drink less, eat less, exercise more” mantra that we should all be following in any case to avoid obesity and its associated health problems. The benefit of potential protective treatment must outweigh the emotional stress that could follow the discovery that one is at increased risk of a nasty brain disease.

Again, the glossy media portrayal of a medical panacea unravels; but science has acquired another small piece in the puzzle of Alzheimer’s pathology.